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College of Osteopathic Medicine of the Pacific

Immunology & Microbiology

Beatrice Saviola Beatrice Saviola, PhD
Associate Professor of Microbiology
COMP-Pomona
bsaviola@westernu.edu
Office#: (909) 469-5373 – Lab#: 469-5436
Research Interests: General focus of Dr. Saviola’s laboratory: Regulation of a Virulence-Associated Acid Response to Mycobacterium Tuberculosis. The bacterium that causes tuberculosis, Mycobacterium tuberculosis, can sense environmental stresses and resist them in order to survive in the body. Creating an acidic environment is one way the body controls bacterial infection. Bacteria can respond to this defense by altering the activity of many of their genes. I have identified in M. tuberculosis a gene, lipF, that is turned on in response to acid. I am studying the basis of this acid response, and anticipate it will provide the groundwork for the eventual identification of a general mechanism by which Mycobacterium tuberculosis can resist acidic stress. To this end I have defined a minimal DNA region upstream of the lipF gene which is transcriptionally upregulated by acidic stress. In addition, I am investigating a nearby gene, Rv3488, as its gene product binds to the lipF promoter region indicating that it may serve as a transcriptional regulator of acidic stress. Information about how virulent M. tuberculosis can respond to environmental stresses that commonly occur within the host could be used to develop therapies that target these mechanisms and make Mycobacterium tuberculosis more sensitive to the immune system’s host defenses.
Hendrik Szurmant Hendrik Szurmant, PhD
Associate Professor of Microbiology
COMP-Pomona
hszurmant@westernu.edu
Office#: (909) 706-3938 – Lab#: (909) 469-8493
Research Interests:

Pathogenic bacteria are some of the most formidable threats to human health. These threats appeared all but eliminated, thanks due to the discovery of powerful antibiotics. The constant exposure of bacteria to these antibiotics has selected for potent multi-drug resistant bacteria, so called superbugs, that are making a strong comeback. To cope with this renewed threat a dedicated effort by the scientific community is needed to identify new drug targets and to generate inhibitors of such targets. The Szurmant laboratory contributes to this endeavor by studying essential aspects of bacterial physiology and signal transduction in model bacteria and selected pathogens. A unique feature of the lab is the integration of information stemming from numerous disciplines, including structural biology, genetics, molecular bioinformatics and biophysics.

Vishwanath Venketaraman Vishwanath Venketaraman, PhD
Associate Professor of Microbiology/Immunology
COMP-Pomona
vvenketaraman@westernu.edu
Office#: (909) 706-3736 – Lab#: (909) 469-6621
Research Interests:

My laboratory studies the pathophysiology of tuberculosis in the context of HIV co-infection and type II diabetes. We are pioneers in reporting that glutathione (GSH) has both antimycobacterial effects and immune enhancing effects and is necessary for the control of Mycobacterium tuberculosis (Mtb) infection. We also reported that the levels of GSH were significantly compromised in macrophages, natural killer (NK) cells and T cells derived from individuals with HIV infection. Decreased levels of GSH in individuals with HIV infection was accompanied by diminished control of intracellular Mtb infection. We then demonstrated that the levels of enzymes that are responsible for the synthesis of GSH such as GSH synthase (GSS), g-glutamyl cysteinyl ligase (GCLC), and GSH reductase (GSR) were significantly reduced in individuals with HIV infection and this reduction correlated with decreased levels of intracellular GSH. We recently conducted a clinical trial in HIV positive individuals to test the efficacy of liposomal glutathione (L-GSH) in restoring the levels of GSH and improving the functions of immune cells. Findings from this study indicate a link between lower levels of GSH and dysregulation in the production of TH1 and TH2 associated cytokines. Furthermore, supplementing individuals with HIV infection for 13 weeks with L-GSH resulted in a significant increase in the levels of TH1 cytokines (IL-1ß, IL-12, IFN-y and TNF-a) along with a substantial decrease in the levels of free radicals and immunosuppressive cytokines (IL-10 and TGF-ß), relative to those in a placebo-controlled cohort. Our studies established a correlation between low levels of GSH and increased susceptibility to Mtb infection via TH2-directed response, which may be relieved with L-GSH supplementation enhancing the TH1 response. I look forward to continuing this important research work (preclinical and clinical studies) and develop immunotherapeutic agents that can be used as adjunct to prevent the development of active tuberculosis in individuals with HIV infection and in people with type II diabetes.